YTHDC2 Double Nickase Plasmid (h): sc-407254-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- YTHDC2 Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- YTHDC2 Double Nickase Plasmid (h) and YTHDC2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting YTHDC2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
YTHDC2 Double Nickase Plasmid (h) | sc-407254-NIC | 20 µg | $410.00 | |||
YTHDC2 Double Nickase Plasmid (h2) | sc-407254-NIC-2 | 20 µg | $410.00 |
YTHDC2 encodes a YTH domain–containing RNA helicase that functions as an m6A reader, coupling recognition of N6-methyladenosine–modified transcripts to ATP-dependent remodeling of ribonucleoprotein complexes. In human cells, YTHDC2 participates in post-transcriptional regulation by influencing mRNA stability, translation efficiency, and RNA surveillance pathways, integrating with broader networks of RNA metabolism. It has been linked to control of cell-cycle–associated transcripts and stress-responsive gene expression programs through selective handling of modified RNAs. Dysregulated YTHDC2 expression or activity has been associated with altered RNA processing signatures observed in multiple disease contexts, supporting its study as a node in epitranscriptomic regulation.
YTHDC2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the YTHDC2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within YTHDC2. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt YTHDC2 function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of YTHDC2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.